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== '''[[ | == '''[[Diabesity]]''' == | ||
''by [[User:Gareth Leng|Gareth Leng]] | ''by [[User:Gareth Leng|Gareth Leng]], [[User:Hannah Frost|Hannah Frost]], [[User:Luke Kennedy Burke|Luke Kennedy Burke]], [[User:Charlie Player|Charlie Player]] and [[User:Katie Rowland|Katie Rowland]] | ||
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''' | The term '''diabesity''' was coined by [https://vpn.ucsf.edu/oby/journal/v19/n3/full/,DanaInfo=www.nature.com+oby2010334a.html Ethan Sims] in 1973, to describe the close relationship between [[diabetes mellitus type 2]] (T2DM) and [[obesity]]. Their findings suggested that by overfeeding young men, with no previous family history of diabetes, the initial signs of diabetes were induced. This excess consuption led to increases in [[insulin]] production, plasma [[glucose]], [[triglycerides]] and eventually impaired glucose tolerance; all signs predisposing one to T2DM and obesity<ref> | ||
Sims EAH ''et al.'' (1973) Endocrine and metabolic effects of experimental obesity in man, ''Recent Prog Horm Res'' 29:457–96</ref><ref>Haslam DW, James WP (2005) Obesity''Lancet'' 366:1197–209</ref> | |||
T2DM is a disorder where cells fail to take up glucose from the blood. Glucose is the fuel for respiration which produces energy for our cells to function properly. Diabetes mellitus is the foremost cause of kidney failure ([[diabetic nephropathy]]), blindness ([[diabetic retinopathy]]), and amputation in adults ([[diabetic neuropathy]]). People with this disease lack the ability to utilize the hormone [[insulin]]. Insulin is produced by the [[pancreas]] after a meal inresponse to increased concentrations of glucose in the blood. The insulin signal attaches to specific receptors on the surface of target cells, causing them to switch on their glucose-transporting machinery. People with T2DM have normal or even elevated levels of insulin in their blood, and normal insulin receptors, but the binding of insulin to its receptors does not turn on the glucose-transporting machinery. | |||
Proteins called [[IRS proteins]] (insulin receptor substrate) bind with the insulin receptor inside the cell. The receptor responds by adding a phosphate group onto the IRS molecules. This rouses the IRS molecules into action, and they activate a variety of processes, including an enzyme that turns on the glucose transporter machinery. When the IRS genes are deliberately inactivated in [[transgenic]] “knockout” mice, T2DM results. However, there are no IRS gene mutations in inherited T2DM; the IRS genes are normal. This suggests that in T2DM something is impeding with the action of the IRS proteins. An estimated 80% of those who develop T2DM are obese. | |||
== | ==Visceral fat accumulation and type 2 diabetes== | ||
Excess visceral adipose tissue increases the risk for T2DM. Excess fat within the [[abdomen]], known as [[visceral adiposity]], creates a serious health risk of metabolic complications independent from accumulation of adipose tissue in other regions: visceral adiposity is related with an increase in ''[[insulin resistance]]'', whereas abdominal subcutaneous fat is not. (''Insulin resistance'' describes the impaired ability of insulin to suppress hepatic glucose output and promote glucose disposal in the periphery.) As T2DM gets worse, patients have higher blood sugar levels ([[hyperglycaemia]]) because the [[pancreatic beta cells]] are unable to make enough insulin. In insulin resistance, normal amounts of insulin are unable to produce a normal response from adipose, muscle and liver cells. Cnop ''et al.'' showed that visceral fat is the best predictor of insulin sensitivity whilst subcutaneous fat establishes leptin levels <ref>Cnop''et al.'' (2002) The concurrent accumalation of intra-adominal and subcutaneous fat explains the association between insulin resistance and plasma leptin concentrations. ''Diabetes'' 51:1005-15</ref> | |||
''[[ | In 1994, a new hormone was found, called [[leptin]], that provides feedback to the brain of the level of fat in the body. Leptin suppresses appetite, but most obese people have very high leptin levels, as leptin is secreted by adipose cells. Therefore, obesity is not generally caused by a deficiency in leptin; instead there seems to be a defect in leptin signalling. Adipocytes also produce an array of other peptides including [[adiponectin]], [[resistin]] and [[TNF alpha]]. They act on peripheral tissues and thereby affect insulin sensitivity and the processes involved in substrate metabolism. | ||
''[[Diabesity|.... (read more)]]'' | |||
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Revision as of 21:50, 24 February 2012
Diabesity
by Gareth Leng, Hannah Frost, Luke Kennedy Burke, Charlie Player and Katie Rowland
The term diabesity was coined by Ethan Sims in 1973, to describe the close relationship between diabetes mellitus type 2 (T2DM) and obesity. Their findings suggested that by overfeeding young men, with no previous family history of diabetes, the initial signs of diabetes were induced. This excess consuption led to increases in insulin production, plasma glucose, triglycerides and eventually impaired glucose tolerance; all signs predisposing one to T2DM and obesity[1][2]
T2DM is a disorder where cells fail to take up glucose from the blood. Glucose is the fuel for respiration which produces energy for our cells to function properly. Diabetes mellitus is the foremost cause of kidney failure (diabetic nephropathy), blindness (diabetic retinopathy), and amputation in adults (diabetic neuropathy). People with this disease lack the ability to utilize the hormone insulin. Insulin is produced by the pancreas after a meal inresponse to increased concentrations of glucose in the blood. The insulin signal attaches to specific receptors on the surface of target cells, causing them to switch on their glucose-transporting machinery. People with T2DM have normal or even elevated levels of insulin in their blood, and normal insulin receptors, but the binding of insulin to its receptors does not turn on the glucose-transporting machinery.
Proteins called IRS proteins (insulin receptor substrate) bind with the insulin receptor inside the cell. The receptor responds by adding a phosphate group onto the IRS molecules. This rouses the IRS molecules into action, and they activate a variety of processes, including an enzyme that turns on the glucose transporter machinery. When the IRS genes are deliberately inactivated in transgenic “knockout” mice, T2DM results. However, there are no IRS gene mutations in inherited T2DM; the IRS genes are normal. This suggests that in T2DM something is impeding with the action of the IRS proteins. An estimated 80% of those who develop T2DM are obese.
Visceral fat accumulation and type 2 diabetes
Excess visceral adipose tissue increases the risk for T2DM. Excess fat within the abdomen, known as visceral adiposity, creates a serious health risk of metabolic complications independent from accumulation of adipose tissue in other regions: visceral adiposity is related with an increase in insulin resistance, whereas abdominal subcutaneous fat is not. (Insulin resistance describes the impaired ability of insulin to suppress hepatic glucose output and promote glucose disposal in the periphery.) As T2DM gets worse, patients have higher blood sugar levels (hyperglycaemia) because the pancreatic beta cells are unable to make enough insulin. In insulin resistance, normal amounts of insulin are unable to produce a normal response from adipose, muscle and liver cells. Cnop et al. showed that visceral fat is the best predictor of insulin sensitivity whilst subcutaneous fat establishes leptin levels [3]
In 1994, a new hormone was found, called leptin, that provides feedback to the brain of the level of fat in the body. Leptin suppresses appetite, but most obese people have very high leptin levels, as leptin is secreted by adipose cells. Therefore, obesity is not generally caused by a deficiency in leptin; instead there seems to be a defect in leptin signalling. Adipocytes also produce an array of other peptides including adiponectin, resistin and TNF alpha. They act on peripheral tissues and thereby affect insulin sensitivity and the processes involved in substrate metabolism.
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